Technical Abstract:
One of the most common symptoms of ozone exposure in plants is known as flecking or stipple, resulting in stimulation of either anthocyanin or phenolic synthesis in the various cells in the epidermis facing high light. Stippled cells change from green to either red or dark purple, whereas in other species, particularly those that produce phenolic-like substances, these cells change from green to dark purple or even brown. Eventually, these cells die and cause wide-spread necrosis over the leaf surface. Similar pigmentation changes also result after pathogen attack, and have led to the hypothesis that ozone induces a generalized pathogen response, probably because both agents result in the accumulation of toxic reactive oxygen species (ROS). Despite the widespread occurrence of pigmentation induction from these agents, almost nothing is known about the potential adaptive significance of such a response. We hypothesize that the synthesis of epidermal pigments reduces the amount of excess light reaching the mesophyll of stressed leaves, limiting further production of ROSs and thereby preventing additional oxidative damage. Spectral scans of injured (>50% stipple) and noninjured leaves of cutleaf coneflower show that injured leaves, when compared to noninjured leaves: absorb less radiation, particularly in the yellow to red wavelengths (550-700 nm), have greater reflection, and transmit more visible radiation. Furthermore, severely injured leaves absorb 50% less radiation in the visible wavelengths than non-injured leaves. Thus the hypothesis that these pigments act as light filters is supported, but whether this reduces ROSs in these injured leaves remains to be investigated.